This invention relates to surgical devices and to methods of using them. In particular, the devices are used to support and to reform myocardial tissue in the region of and across an infarct. The devices provide support to the infarct in varying degrees by attachment of the inventive device to the myocardium at sites adjacent the infarct. A supporting component across the infarct, between the heart attachment sites, provides support to the myocardial wall and to the infarcted region. Optionally, but preferably, the supporting component includes a time-delay element that variously may allow the device to be safely manipulated and introduced onto the myocardial surface and then to change the distance between the ends of the support member or the amount of infarct support over time.
This invention relates to devices and processes for treating, in particular, ischemic heart diseases, particularly myocardial infarction. The term xe2x80x9cmyocardial infarctionxe2x80x9d generally refers to the death of that tissue resulting from either inadequate blood supply or an absolute lack of blood supply to that tissue region. Classically, a xe2x80x9cheart attackxe2x80x9d occurs with the sudden onset of specific symptoms, followed by a specific series of electrocardiographic changes and a rise in serum levels of enzymes released from the myocardium. Total occlusion of a major coronary artery by thrombosis creates an infarcted area involving virtually the full thickness of the ventricular wall in the region of the heart supplied by the blocked artery. The occlusion of the coronary artery may occur more slowly and not completely block the artery. The resulting infarction then occurs over a significant period of time and may be less localized.
In the United States, myocardial infarction occurs in upwards of two million people a year. Less than half of those persons are hospitalized and a quarter to a third of them die suddenly outside of the hospital.
Coronary artery thrombosis almost always occurs at the site of an atheromatous plaque. Although plaque is present, it does not typically severely narrow the lumen of the affected artery before the thrombosis occurs. The formation of the thrombus is caused by a variety of events and likely may be considered to be the formation of a breakage in the intimal lining or hemorrhage within the plaque. Generally, plaques that are amenable to such fissuring are soft, rich in lipid, and formed in such a way that a fibrous cap overlies the softer lipid material. The fissure frequently occurs at the junction of the fibrous cap and a normal intima. As is a case with any vascular injury of this type, the response is an aggregation of platelets. The platelets begin a cascade of the release of thromboxane, promoting further platelet aggregation, coronary vasoconstriction, further reduction of blood flow, and formation of a thrombus. These coronary occlusions occur without warning signs in most instances, although physical activity and stress may have some role in causation.
In any case, these coronary accidents are easily detectable by electrocardiogram. Similarly, the treatment of acute myocardial infarction is typically via medication. Treatment of pain, perhaps by administering sublingual nitroglycerin is common. The goal of medicinal therapy in such cases is the opening of the partially closed artery. Administration of thrombolytics such as streptokinase, alteplace (recombinant tissue plasminogen activatorxe2x80x94rt-PA), and anistreplase (anisoylated plasminogen streptokinase activated complex or APSAC) may be had. In some instances, angioplasty is administered, typically without thrombolysis, but on rare occasions with such a drug.
It is uncommon to treat infarcts with surgery unless there have been anatomic complications of the myocardial infarction, e.g., ventricular septal rupture, mitral regurgitation, ventricular aneurysms, ATC. Two procedures for dealing with myocardial infarcs via surgery are the Batista Procedure and the Dor Procedure, named after the surgeons who first performed them. In the Batista Procedure, the surgeon resects a portion of the heart to change its shape to a more correct cone shape. The Batista Procedure removes both healthy tissue and tissue not so healthy. The procedure is said not to be in favor due to high complication rates.
The Batista Procedure was replaced by a surgery known as the Dor Procedure. The Dor Procedure is less aggressive and apparently more effective. The Dor Procedure is typically used after an aneurysm forms following the presence of an infarct. The Dor Procedure is also called xe2x80x9cendoventricular circular patch plastyxe2x80x9d or EVCPP. The procedure creates a looped stitch pattern around a dead, scarred aneurysm to shrink the dead area. Any remaining defect may be covered by a patch made from DACRON or tissue. The aneurysm scar is closed over the outside of the patch to make the overall site more stable.
A variation of the Dor Procedure is called the SAVR Procedure, which stands for Surgical Anterior Ventricular Remodeling. This procedure opens the affected ventricle through the xe2x80x9cakineticxe2x80x9d segment. A surgeon feels the beating heart and detects, using the fingers, where the heart muscle is not working. A suture is placed at the junction of a beating muscle and non-beating muscle that is typically semicircular, purse-string suture shape. A patch is then installed.
There are a variety of devices which are applied to the heart for treatment of congestive heart failure (CHF). Patents owned by Abiomed (U.S. Pat. Nos. 6,224,540; 5,800,528; 5,643,172) show a girdle-like device situated to provide structure to a failing heart. U.S. patents owned by Acorn Cardiovascular, Inc. (U.S. Pat. Nos. 6,241,654; 6,230,714; 6,193,648; 6,174,279; 6,169,922; 6,165,122; 6,165,121; 6,155,972; 6,126,590; 6,123,662; 6,085,754; 6,077,218; 5,702,343) show various devices, also for treatment of CHF, which typically include a mesh sock-like device placed around the myocardial wall. U.S. patents to Myocor, Inc. (U.S. Pat. Nos. 6,264,602; 6,261,222; 6,260,552; 6,183,411; 6,165,120; 6,165,119; 6,162,168; 6,077,214; 6,059,715; 6,050,936; 6,045,497; 5,961,440) show devices for treatment of CHF generally using components which pierce the ventricular wall.
None of the devices described in any of these patents suggests the devices and methods disclosed here.
This invention is a heart tissue supporting device comprising a.) at least one first heart tissue adherence region (each adapted to adhere to selected first heart tissue regions on a heart surface), b.) at least one second heart tissue adherence region, separated from the first heart tissue adherence regions and each adapted to adhere to selected second heart tissue regions on a heart surface, and c.) at least one support-providing member situated variously to maintain support to the tissue located between the first heart tissue adherence regions and the second heart tissue adherence regions.
The first and second heart tissue adherence regions may be at least partially surrounded by a region that is substantially non-adhering to heart tissue. The tissue support-maintaining member is sized and placeable to maintain the distance between the first and second heart tissue contact regions. The device may include a connector strap that is substantially non-adhering to heart tissue and is configured to connect the first and second heart tissue adherence regions around the heart not adjacent the infarct to form a loop surrounding the heart. The portions of the device that do not adhere to heart tissue may be made from non-adherent materials such as woven or non-woven polymeric fabrics, e.g., polyfluorocarbons and polyolefins, such as polytetrafluoroethylene (PTFE or TFE), ethylene-chlorofluoroethylene (ECTFE), fluorinated ethylene propylene (FEP), polychlorotrifluoroethylene (PCTFE), polyvinylfluoride (PVF), polyvinylidenefluoride (PVDF), polyethylene (LDPE, LLDPE, and HDPE), and polypropylene.
The portions of the device that should adhere to the heart may be made of materials known to adhere, adhering materials selected to allow ingrowth such as woven or non-woven polymeric fabrics desirably selected from polyethyleneterephthalate, cotton, and expanded polyfluorocarbons having internodal spacing suitable for intergrowth.
The device includes at least one support-maintaining member, often having a spring with opposing ends attached between the at least one first heart tissue adherence region and the at least one second heart tissue adherence region. The springs may be coiled or flat or other suitable shape. The support-maintaining member further desirably includes a time-delay member adapted to provide a period of time between the introduction of the device onto the heart and the initiation of a movement of the first heart tissue adherence region towards the second and/or to provide a period of time over which the distance between the first heart tissue adherence region and the second heart tissue adherence region varies.
The time-delay member may be coated with, embedded in, or be formed of a suitable biodegradable material.
The first or second heart tissue adherence regions may have surfaces selected to allow or enhance ingrowth of heart tissue into those regions. The regions may be, e.g., not smooth, roughened, nubbed, perforated, etc.
As appropriate, the surfaces of the device, e.g., the heart tissue supporting member, the time-delay member, and the first and second heart tissue adherence regions, may be treated with at least one angiogenesis composition.
The first and second heart tissue adherence regions may be made to adhere to the heart tissue in a variety of ways, e.g., by mechanical fasteners, by ingrowth, by adhesives, or other materials, devices or procedures that cause the device component to adhere to the heart.
The invention includes methods for use of the device itself, methods of supporting a localized or regional area of a heart particularly where that region includes an infarct or region that has been surgically altered. Procedures typically include the steps of adhering a first tissue contact area of a supporting member to the myocardial wall at a first tissue site adjacent the infarct or other region to be supported, adhering a second tissue contact area of the supporting member to the myocardial wall at a second tissue site adjacent the infarct or other region to be supported but adapted for positioning the supporting member across the region of concern, and maintaining the distance between or advancing the first tissue contact area towards the second tissue contact area. The procedures may involve adhesively connecting the first and second tissue contact areas respectively to first and second tissue sites or by allowing ingrowth or by mechanically fastening a contact area to the tissue site. The step of advancing the two tissue contact area towards each other may take place as a result of the erosion of a bioerodible material situated between those first and second tissue contact areas. The advancing step may comprise eroding a bioerodible material time-delay member associated with the support-maintaining member in such a way that it tends to tend to hold the spring in extension until after functional biodegradation in the human body. The advancing step may include eroding the support-maintaining member itself when that member is made up of a bioerodible material.
Finally, the invention includes a fastener made up of a shaft terminating at one end in a tissue piercing end and having a collar end at the opposite end, a collar slidable on the shaft, and a braided member concentric to the shaft, affixed to the shaft substantially adjacent the tissue piercing end. The fastener operates in the following way. The collar on the on the shaft slides towards the tissue piercing end and expands the braided member. The region between the collar and the braided member is appropriate for fastening. The braided member may be affixed to the collar at the end opposite the tissue piercing end. Desirably, the fastener includes a stop for affixing the shaft to the collar after the braided member has been expanded.